Inhibition of microRNA-203 by oncogenic HRas mutations promotes skin cancer initiation.

Oncogenic BRAF causes genome duplication and reversible growth arrest in human melanocytes that is conditional on microRNA expression and differentiation state.

microRNAs can serve as a surveillance system to repress nonsense mRNAs by recognizing miRNA-responsive elements in the open reading frame region downstream of the premature termination codon.

microRNA-1 plays an essential role in the development and functioning of the heart by ensuring that genes for striated, rather than smooth, muscle are expressed there.

The deletion of Ddx6 results in the translational upregulation, but not transcript stabilization, of microRNA targets in embryonic stem cells while largely phenocopying the overall impact of global microRNA loss.

MicroRNA-based direct conversion of human fibroblasts to neurons is applicable to fibroblasts from donors ranging in age from neonatal to centenarian, allowing the generation of neurons that maintain the age-associated signatures of the starting fibroblasts.

Extracellular vesicles derived from natural killer cells contain a specific repertoire of microRNAs that promote Th1 responses.

Lymphatic-enriched microRNA miR-204 is required for lymphatic development through its effects on the key lymphatic transcription factor NFATC1.

A cell-free reaction that reconstitutes the selective sorting of a miRNA into exosomes reveals an RNA-binding protein, YBX1, as a critical sorting factor.

Coordinated microRNAs activity induced by VEGF represses cell proliferation and favors cell migration at the onset of sprouting angiogenesis in endothelial cells.